ArticleOncogene2026
Methylation-driven SOX18 nuclear translocation by IGF2BP1-stabilized METTL21A promotes lymphatic metastasis in gastric cancer.
Article in Oncogene, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Gastric cancer (GC) is frequently associated with lymph node metastasis, which contributes to a poor prognosis; however, the underlying molecular mechanisms remain incompletely understood. In this study, we identify the N6-methyladenosine (m⁶A) reader IGF2BP1 as a critical driver of lymphatic metastasis in GC. IGF2BP1 is significantly upregulated in GC tissues with lymph node metastasis and is correlated with adverse clinical outcomes. Mechanistically, IGF2BP1 binds to the m⁶A-modified 3' untranslated region (3'UTR) of METTL21A mRNA, thereby enhancing its mRNA stability and expression levels. METTL21A, a non-histone lysine methyltransferase, interacts with and methylates the transcription factor SOX18, facilitating its nuclear translocation without altering protein stability. Once in the nucleus, SOX18 directly activates the transcription of CXCL12. Secreted CXCL12 promotes lymphangiogenesis and facilitates lymphatic metastasis through CXCR4 signaling. Functionally, both IGF2BP1 and METTL21A enhance tube formation and migration of lymphatic endothelial cells and promote lymphatic metastasis in GC. Notably, METTL21A knockout abolishes IGF2BP1-induced lymphangiogenesis, whereas SOX18 depletion eliminates the pro-lymphangiogenic effects of IGF2BP1. Our findings reveal a previously unrecognized signaling axis-IGF2BP1-METTL21A-SOX18-CXCL12-that links m⁶A-dependent post-transcriptional regulation with methylation-dependent transcriptional activation, offering potential therapeutic targets for the prevention of lymphatic metastasis in gastric cancer.
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Registered trials
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